Leg vein thrombosis

Leg vein thrombosis – deep vein thrombosis

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Leg vein thrombosis is a condition in which a blood clot (thrombus) forms in a deep vein in the leg. This can restrict blood flow and cause swelling, pain, redness, and warmth in the affected leg. Leg vein thrombosis can also lead to serious complications such as pulmonary embolism if part of the thrombus breaks away and travels to the lungs. Pulmonary embolism is an often fatal disease. Thrombophlebitis must be distinguished from deep vein thrombosis. However, you should not make this distinction yourself, but rather contact an experienced specialist in vascular surgery and phlebology and have it examined clinically, with ultrasound and through special laboratory tests. Thrombophlebitis is usually less dangerous than leg vein thrombosis, but in rare cases it can also lead to deep vein thrombosis or pulmonary embolism.

Symptoms of deep vein thrombosis

Symptoms of deep vein thrombosis can vary depending on the location and extent of the clot, but some common signs include:

Swelling of the affected leg, usually on one side
Pain in the leg, often in the calf or foot
Redness, warmth, or discoloration of the skin over the clot
Feeling of tension or cramps in the leg

These symptoms do not always occur or are only mild. Sometimes those affected only notice the thrombosis when it leads to a complication such as a pulmonary embolism. A pulmonary embolism is a life-threatening emergency caused by sudden Atemdistress, chest pain, coughing or coughing up blood. If you have one or more of these symptoms, you should definitely see a doctor to determine the cause and begin appropriate treatment.

Treatment of leg vein thrombosis

Deep vein thrombosis can be treated with medication, compression stockings, or, in rare cases, surgery. Treatment aims to prevent the clot from growing or detaching and to reduce the risk of subsequent damage. Treatment can be on an outpatient or inpatient basis, depending on how well the patient needs to be monitored. Treatment usually includes the following measures:

Blood thinning medications (anticoagulants), which prevent the formation of further blood clots and promote the dissolution of the existing thrombus. These medications can be given as tablets or injections. Drug therapy can partially or completely dissolve the clot. The extent of the thrombosis, the length of the affected vein and the effectiveness of the anticoagulant therapy are decisive as to whether the veins closed by thrombosis will reopen with drug therapy.
compression stockings or bandages that apply gentle pressure to the leg and improve blood flow. These should be worn for several months.
Exercise instead of bed rest: In the past, every patient with thrombosis had to lie in bed to avoid the risk of a pulmonary embolism. Today's basic principles are different and exercise is usually permitted under effective blood thinning and compression therapy to promote blood flow and reduce swelling. However, this should only be done under the guidance of a doctor and with effective anticoagulation - blood thinning - and compression treatment.
Painkiller only in the short term if the pain is severe
Surgical interventions for thrombosis are only necessary in rare cases if the medication does not work or is not tolerated. The thrombus can be removed mechanically (thrombectomy) or a device can be used to prevent it from reaching the lungs (vena cava filter). Who should undergo surgery is decided depending on the doctor, the clinic and their options. If the thrombosis is diagnosed in an internal medicine department or in an outpatient venous practice, conservative measures are often prescribed. If the technical and personnel requirements for a venous thrombectomy are met, then the indication for surgical removal of the thrombosis can be made, thereby preventing lifelong venous insufficiency. Surgical therapy also depends on the patient's will: how active he is, how old he is, whether he has been informed about the risks of pulmonary embolism with or without surgery. Therefore, therapy for severe thrombosis is always a joint decision between the vascular surgeon and the patient.

Duration of treatment for deep vein thrombosis

The duration of treatment for leg vein thrombosis depends on various factors, such as the location, extent and cause of the thrombosis and, above all, on the type of treatment chosen. Treatment for leg vein thrombosis can be done on an outpatient or inpatient basis, depending on how well the patient needs to be monitored. The duration of treatment varies depending on the individual case, but on average you can expect the following periods:

The blood thinning medication must be taken for at least three to six months.
The compression stockings or bandages must be worn for at least six months.
Movement of the leg should be started as soon as possible and continued regularly
The surgical procedures usually last one to two hours and usually require a short hospital stay of one to two days

Causes and risks of thrombosis

The risk factors for deep vein thrombosis are several factors that increase the likelihood of a blood clot forming in a deep vein of the leg and obstructing blood flow. Risk factors include:

Damage to the vessel wall: This can be caused by injury, inflammation, infection or tumors that irritate or change the inner walls of the veins.
Reduced blood flow speed: This can occur due to a lack of exercise, sitting or lying down for long periods of time, varicose veins or heart failure, which slow or hinder the return of blood to the heart.
Increased tendency of the blood to clot: This can be caused by genetics, hormones, medications, cancer or other diseases that disrupt the balance between clotting factors and anticoagulants in the blood.

Some risk factors are temporary, such as surgery, pregnancy or a long trip. Other risk factors are permanent, such as older age, obesity or smoking. The risk factors can also reinforce each other and increase the risk of thrombosis.

Diagnosis of leg vein thrombosis

To diagnose deep vein thrombosis - phlebothrombosis - there are various methods that can be used depending on suspicion and availability. The most important are:

The History and clinical examination, the “visual diagnosis” – that is, the experienced impression of the affected patient, whereby the doctor asks about possible risk factors, symptoms and findings and examines the affected leg. He can look out for typical signs such as swelling, redness, pain or overheating. However, these signs are not always present or clear.
The Duplex sonography, which is an ultrasound scan that shows both the structure and function of the veins. The doctor can see whether the vein is blocked by a blood clot or not. This method is quick, easy and risk-free and is considered the method of choice for diagnosing deep vein phlebothrombosis.
The D-dimer test, which is a blood test that detects the breakdown products of blood clots in the blood. An increased value can indicate a thrombosis, but can also have other causes. A normal value most likely excludes thrombosis. This test is often used in combination with duplex sonography.
The Phlebography, which is an X-ray test in which a contrast agent is injected into the vein to make it visible. The doctor can see whether the vein is patent or narrowed. This method is considered very accurate, but also invasive and associated with side effects. It is therefore only rarely used when other methods are not sufficient or not available.

To diagnose thrombosis, there are various genetic tests that can analyze blood clotting factors. The most important are:

The Factor V Leiden mutation, which is also known as APC resistance, is determined by APC genotyping. It is a hereditary disease that disrupts blood clotting. This means those affected have a higher risk of getting a blood clot (thrombosis). The disease is usually caused by a genetic mutation in blood clotting factor V (read: five). The mutation means that factor V can no longer be properly cleaved by the activated protein C (APC), which leads to an increased tendency to clot. The mutation can be detected with a genetic test.
The Prothrombin mutation G20210A, which is an inherited disease that also disrupts blood clotting. This means that those affected have a higher risk of developing both venous and arterial thrombosis. The disease is caused by a genetic mutation in the regulatory region of the prothrombin gene, which leads to increased expression of the gene and thus to an accumulation of prothrombin in the plasma. The mutation can be detected with a genetic test.
The MTHFR mutation, which is an inherited disease that affects the enzyme methylenetetrahydrofolate reductase (MTHFR). The enzyme plays an essential role in homocysteine metabolism. Homocysteine is a breakdown product of methionine metabolism, which at elevated levels can lead to damage to the vessel walls and platelet activation. The mutation can be detected with a genetic test.

These genetic tests are relevant for the diagnosis of thrombosis because they can determine the individual risk of thrombosis. However, they are not the only deciding factor, but must always be considered in combination with other factors such as the history of the disease, the symptoms and the laboratory values. In addition, they can only indicate a genetic predisposition, but cannot predict whether and when a thrombosis will occur. It is therefore important to take other preventive measures to reduce the risk of thrombosis, see above.

In addition to the genetic tests we have already mentioned to you, there are other laboratory tests that can increase the risk of thrombosis. Dazu gehören ¹ ²:

The increased concentration of fibrinogen, an important clotting factor that enables the formation of fibrin threads. Fibrinogen can be increased due to inflammation, infections, smoking or stress and lead to an increased tendency to clot.
The increased concentration of factor VIII, another clotting factor that promotes the activation of factor X and thus the formation of thrombin. Factor VIII can be increased due to pregnancy, hormone intake, cancer or other diseases and can double the risk of thrombosis.
Protein C deficiency (Fibrin formation disturbed)
Protein S deficiency (Fibrin formation disturbed)
Factor VIII increase in antihemophilic globulin A - promotes fibrin formation and thus thrombosis
von Willebrand-Jürgens factor (vWF; coagulation factor VIII-associated antigen or von Willebrand factor antigen, vWF:Ag)
platelet count
The increased concentration of lipoprotein (a), a blood fat that is structurally similar to plasminogen. Plasminogen is an enzyme that helps dissolve blood clots. Lipoprotein (a) can inhibit the binding and activation of plasminogen to fibrin and thus promote clotting.
The increased concentration of homocysteine, an amino acid that is produced when the metabolism of folic acid and vitamin B12 is disturbed. Homocysteine can damage vessel walls and increase platelet activation, increasing the risk of arterial and venous thrombosis.
The increased concentration of antiphospholipid antibodies, a group of autoantibodies directed against phospholipids. Phospholipids are components of cell membranes and play a role in blood clotting. Antiphospholipid antibodies can disrupt the function of phospholipids and lead to an increased tendency to clot. This is called antiphospholipid syndrome.
Lupus anticoagulant

These laboratory tests can indicate the risk of thrombosis, but cannot determine it alone. They must always be considered in conjunction with other factors such as history, symptoms and imaging studies. In addition, they can only reflect a momentary situation, but cannot predict whether and when a thrombosis will occur. It is therefore important to also take other preventive measures to reduce the risk of thrombosis.

Leg vein thrombosis